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My research aims to define the role of neutrophil-endothelial cell interactions in regulating pulmonary inflammation. Much of our understanding of neutrophil-pulmonary vascular endothelial cell interaction, and the mechanisms underlying the recruitment of leukocytes into the lung, has been extrapolated from studies undertaken in the systemic circulation. However, substantial differences exist between the pulmonary and systemic circulations, including the site of leukocyte migration (pulmonary capillaries rather than post-capillary venules), the importance of physical entrapment of neutrophils in the lung microcirculation over adhesion/rolling events, and major differences in the repertoire of endothelial ligands expressed. I have previously demonstrated that the healthy human pulmonary vasculature plays a critical role in host defence by selectively trapping primed neutrophils, facilitating their de-priming, and later releasing them back into the pulmonary circulation in a quiescent state, and furthermore that this homeostatic mechanism fails in patients with acute respiratory distress syndrome (ARDS). I am currently delineating the critical neutrophil-endothelial cell interactions occurring during these processes, so we may better develop efficacious therapies for pulmonary inflammation in the critically ill.

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